There has long been an interest in the structure of adipose tissue as it relates to a possible role in obesity. Brown adipose tissue is the main effector of cold- and diet-induced thermogenesis in mammals, such as rodents. See Foster et al., Can. J. Physiol., Vol. 56, 110 (1978) or Rothwell et al., Nature (London), Vol. 281, 31 (1979). The process of thermogenesis can represent a major expenditure of energy and play an important role in overall energy balance. Because brown adipose tissue has been demonstrated in humans of all ages and is often atrophied or quiescent in obese animals, much interest has recently been directed towards development of compounds that stimulate the thermogenesis metabolic response as possible anti-obesity agents.
Brown adipose tissue metabolism is primarily controlled by norepinephrine released from the sympathetic nerve terminals that act through .beta.-adrenergic receptors. Both .beta..sub.1 - and .beta..sub.2 -adrenergic receptor subtypes are present in rat brown adipose tissue; however, pharmacological studies with novel thermogenic .beta.-adrenergic agonists have suggested the existence of an atypical .beta.-adrenergic receptor in the brown adipose tissue that mediates lipolysis (breakdown of fat). Parallel studies have also suggested the presence of atypical .beta.-adrenergic receptors with similar pharmacological properties in white adipose tissue, the digestive track, and in skeletal muscle.
Accordingly, there is a need in the art for isolation and understanding of the fat cell .beta. receptor or receptors which are related to the thermogenesis process. Such an isolation of the .beta.-adrenergic receptor(s) would allow for the diagnosis of obesity, the treatment of obesity, the testing of medications for their effectiveness in stimulating the thermogenesis metabolic response in obesity patients.